Renal Biochemistry and Urinalysis: Interpreting Kidney Function Tests

By Dr. Zubair Khalid, DVM, MS, PhD · 2026-08-11

Key Takeaways

• Serum creatinine and blood urea nitrogen (BUN) are common surrogates for glomerular filtration rate (GFR) but are insensitive for early kidney disease, with creatinine requiring approximately 75% nephron loss and BUN being influenced by factors beyond renal function such as protein intake and hydration status.
• Symmetric dimethylarginine (SDMA) offers an earlier indicator of declining GFR than creatinine, is less affected by muscle mass, and serves as a valuable adjunct for detecting early renal dysfunction, though it does not replace urinalysis for localization.
• Urinalysis is critical for localizing renal lesions; urine specific gravity assesses concentrating ability (isosthenuria with azotemia indicates renal failure), while urine sediment analysis identifies casts and cells indicative of tubular injury, and the urine protein:creatinine ratio (UPC) quantifies glomerular protein loss, a negative prognostic indicator in stable CKD.
• The International Renal Interest Society (IRIS) staging system categorizes chronic kidney disease (CKD) based on fasting serum creatinine, proteinuria substaging (UPC), and blood pressure substaging, providing a framework for prognosis and treatment decisions.
• Distinguishing acute kidney injury (AKI) from chronic kidney disease (CKD) is crucial, with AKI often presenting with larger kidneys and a recent inciting event, while CKD is suggested by a history of weight loss, anemia, and palpably small kidneys.
• Common interpretation errors include over-reliance on single creatinine values without considering muscle mass or hydration, dismissing isosthenuria with normal creatinine as insignificant, and misinterpreting dipstick proteinuria without sediment analysis or UPC quantification.

This article provides a diagnostic framework for interpreting renal biochemistry and urinalysis in dogs and cats, with reference to other domestic species where relevant. It serves the practicing veterinarian who must distinguish prerenal, renal, and postrenal azotemia, recognize early kidney disease before irreversible damage accumulates, and stage chronic kidney disease using current consensus systems. The content focuses on test selection, interpretation pitfalls, and the physiologic basis for each diagnostic decision, and it excludes specific treatment protocols.

The central diagnostic question is whether the kidney is functioning adequately, and if not, where the lesion lies. No single test answers this completely. Serum creatinine and urea nitrogen reflect function, not damage, and both have substantial limitations. Urinalysis provides complementary information about concentrating ability, protein loss, and sediment findings that localize disease to the glomerulus, tubules, or interstitium. Newer biomarkers such as symmetric dimethylarginine (SDMA) address some gaps in conventional testing, particularly for early detection of reduced glomerular filtration rate (GFR). The conventional tests of kidney damage and function in blood and urine are widely used, but each has important limitations, and additional markers of GFR and of glomerular and tubular damage are desirable for earlier detection when therapy is most effective, as reviewed in the veterinary biomarker literature Hokamp and Nabity, renal biomarkers in domestic species.

At a Glance

Physiology of Renal Function Tests

The kidney filters plasma at the glomerulus, reabsorbs solutes and water along the tubules, and secretes selected waste products. GFR is the physiologic parameter that best reflects overall excretory function, but it cannot be measured directly in clinical practice. Endogenous markers such as creatinine and SDMA are used as surrogates. Their serum concentrations rise when GFR falls, but the relationship is hyperbolic instead of linear. A 50% reduction in GFR may produce only a modest increase in serum creatinine within the reference interval, whereas further decline produces disproportionately large increases. This explains why creatinine is insensitive for early disease and why a normal value does not exclude significant functional loss.

Renal perfusion is a separate determinant of function. Acute kidney injury (AKI) frequently involves reduced cortical perfusion, and imaging techniques such as arterial spin labeling magnetic resonance imaging can demonstrate serial perfusion changes that correlate with histologic injury and with inulin and para-aminohippuric acid clearance in experimental models Hueper et al, arterial spin labeling to monitor renal perfusion impairment. These methods are research tools, but they underscore that functional tests reflect perfusion as well as parenchymal health. A dehydrated patient with prerenal azotemia has reduced renal blood flow and a transiently reduced GFR that corrects with volume restoration.

The kidney also has metabolic and endocrine functions that influence systemic physiology. The liver and kidney interact bidirectionally in disease states. Acute kidney injury can impair hepatic synthetic function, acute phase responses, and drug metabolism, a phenomenon termed renohepatic crosstalk Lane et al, renohepatic crosstalk. This matters clinically because a patient with AKI may show liver enzyme elevations or altered drug clearance that is not primary hepatic disease. Conversely, chronic liver disease can affect urea production and confound BUN interpretation.

Serum Creatinine: Strengths and Limitations

Creatinine is produced from muscle creatine and phosphocreatine at a relatively constant rate and is excreted almost entirely by glomerular filtration, with minimal tubular secretion in dogs and cats. Its serum concentration is therefore a practical GFR surrogate. The limitations are well documented. Muscle mass directly influences the baseline value, so a cachectic or heavily muscled patient may have a creatinine concentration that misrepresents GFR. The same GFR can produce different creatinine values in different patients, and serial changes within an individual are more informative than a single value compared with a population reference interval. The veterinary biomarker review highlights these limitations and discusses strategies for improved interpretation based on past literature and recent studies Hokamp and Nabity, renal biomarkers in domestic species.

Creatinine is also slow to respond to acute changes. After an acute insult, creatinine may not peak for 48 to 72 hours, and a single early measurement can underestimate injury severity. Serial measurements are required to establish the trajectory. In experimental models of AKI, histologic injury can be present when functional markers are still within reference limits, reinforcing that creatinine is a lagging indicator.

Blood Urea Nitrogen: Physiology and Confounders

Urea is synthesized in the liver from ammonia, which is derived largely from dietary protein and tissue catabolism. It is freely filtered at the glomerulus, and a variable fraction is reabsorbed in the tubules, particularly when urine flow is slow. This reabsorption makes BUN a less reliable GFR marker than creatinine. Prerenal azotemia, caused by dehydration or reduced renal perfusion, increases tubular urea reabsorption and can elevate BUN out of proportion to creatinine. High protein diets, gastrointestinal hemorrhage, and catabolic states increase urea production. Hepatic insufficiency decreases urea production and can mask azotemia.

The BUN to creatinine ratio is frequently used to distinguish prerenal from renal azotemia, but it must be interpreted cautiously. A ratio above 20 is suggestive of prerenal or postrenal causes, while a ratio near 10 to 15 is more consistent with primary renal disease. The overlap is substantial, and urine specific gravity is a more reliable discriminator. A concentrated urine in an azotemic patient supports prerenal azotemia, whereas isosthenuria with azotemia indicates renal failure. The ratio is best used as a secondary clue instead of a primary diagnostic criterion.

Symmetric Dimethylarginine

SDMA is a methylated arginine derivative released during protein turnover and excreted primarily by renal filtration. It correlates with GFR and has two practical advantages over creatinine. First, it is less influenced by muscle mass, so it may be more reliable in cachectic or muscular patients. Second, it appears to rise earlier than creatinine as GFR declines, allowing earlier detection of reduced function. The evidence base in dogs and cats supports its use as an adjunct to creatinine, but it is not a substitute for urinalysis. A normal SDMA does not exclude structural kidney damage, and an elevated SDMA should prompt further investigation instead of immediate diagnosis. Reference intervals vary by laboratory and methodology, and the ASVCP quality assurance guidelines provide a framework for validating and interpreting such assays in practice ASVCP quality assurance and laboratory standards guidelines.

Urinalysis as a Localizing Test

Urinalysis provides information that blood tests cannot. Urine specific gravity assesses tubular concentrating ability, which is one of the earliest functions lost in chronic kidney disease. A urine specific gravity above 1.030 in a dog or 1.035 in a cat with azotemia indicates that the tubules are responding to antidiuretic hormone and that the azotemia is likely prerenal. Isosthenuria, a specific gravity between 1.008 and 1.012, with azotemia confirms renal failure. A fixed specific gravity in the absence of azotemia may indicate reduced renal reserve and warrants monitoring.

Proteinuria is detected by dipstick or sulfosalicylic acid precipitation and quantified by the urine protein to creatinine ratio. Persistent proteinuria in a patient with stable chronic kidney disease is associated with faster progression. The source of protein can be inferred from molecular weight. High and intermediate molecular weight proteins in the urine indicate glomerular damage, while low molecular weight proteins and enzymes suggest tubular damage from decreased reabsorption, direct tubular injury, or both Hokamp and Nabity, renal biomarkers in domestic species. Sediment examination identifies casts, cells, and crystals that localize the lesion further. An active sediment with granular or cellular casts supports tubulointerstitial injury, while a bland sediment with significant proteinuria points toward glomerular disease.

Staging Chronic Kidney Disease: The IRIS Framework

The International Renal Interest Society (IRIS) staging system provides the standard framework for classifying chronic kidney disease (CKD) in dogs and cats. Staging is based on fasting serum creatinine concentration measured on two or more occasions in a stable patient with consistent hydration status. The system assigns stages 1 through 4, with substaging for proteinuria and systemic blood pressure.

Creatinine thresholds are not absolute boundaries. A dog with a creatinine of 1.3 mg/dL and isosthenuria, renal proteinuria, and histologically confirmed nephropathy is IRIS stage 1, not stage 0. Conversely, a dehydrated dog with a creatinine of 1.5 mg/dL that concentrates urine normally after rehydration is not necessarily stage 2. The staging decision requires integration of serial creatinine values, urinalysis findings, and clinical assessment. The ASVCP quality assurance guidelines emphasize that laboratory reference intervals vary by analyzer and population, so results should be interpreted against the reference interval of the laboratory actually used.

Proteinuria Substaging

Proteinuria is substaged using the urine protein-to-creatinine ratio (UPC) on a sample collected when the urine is not contaminated by hemorrhage or inflammation. A UPC below 0.2 in dogs and below 0.4 in cats is considered non-proteinuric. Values above 2.0 in dogs and above 0.4 in cats with confirmed renal disease warrant intervention. Borderline values between 0.2 and 0.5 in dogs should prompt rechecking, as transient proteinuria from exercise, fever, or urinary tract infection can confound interpretation.

Blood Pressure Substaging

Arterial blood pressure is measured by Doppler or oscillometric methods with the patient calm and in a consistent position. Systolic pressure above 160 mmHg sustained over multiple visits, or above 180 mmHg on a single visit, indicates risk of target organ damage. Hypertension substaging modifies prognosis and treatment decisions independently of creatinine stage.

The Diagnostic Sequence in Suspected Renal Disease

The workup proceeds in a defined order. First, confirm that azotemia is renal in origin by assessing urine specific gravity (USG) on a sample collected before fluid therapy. A USG above 1.030 in dogs and above 1.035 in cats with concurrent azotemia suggests prerenal or postrenal causes. A USG below these thresholds with azotemia supports intrinsic renal disease, provided the patient is not receiving diuretics, glucocorticoids, or fluids.

Second, distinguish acute from chronic disease. Chronic kidney disease is suggested by a history of weight loss, poor body condition, nonregenerative anemia, and palpably small or irregular kidneys. Acute kidney injury (AKI) presents with larger or normal-sized kidneys, often with a recent inciting event such as toxin exposure, ischemia, or drug administration. The distinction matters for prognosis and monitoring intensity. The review of renal biomarkers in domestic species notes that conventional tests such as serum creatinine and urea nitrogen have important limitations in both sensitivity and specificity, and that additional markers may improve early detection.

Third, localize the lesion. Glomerular disease produces proteinuria with relatively preserved concentrating ability early in the course. Tubular disease produces isosthenuria early, often with glucosuria, aminoaciduria, or enzymuria in the absence of hyperglycemia. The presence of high- and intermediate-molecular-weight proteins in urine indicates glomerular damage, while low-molecular-weight proteins and enzymes suggest tubular injury, as described in the renal biomarker review.

Urinalysis Interpretation Checklist

The following checklist structures the urinalysis interpretation for suspected renal disease. Each finding is interpreted in context, not in isolation.

• Specific gravity: Interpret before fluid therapy. Isosthenuria (1.008 to 1.012) with azotemia strongly supports renal failure. A fixed USG across serial samples indicates loss of concentrating and diluting capacity.
• Protein: Dipstick protein is a screening test only. Confirm with sulfosalicylic acid precipitation or UPC. A negative dipstick with dilute urine can miss significant proteinuria.
• Glucose: Glucosuria with normal blood glucose indicates proximal tubular dysfunction. Confirm with blood glucose measurement.
• Sediment: Active sediment with bacteria, white blood cells, or red blood cells can cause proteinuria and should be treated before UPC interpretation. Casts, particularly granular or cellular casts, support tubular injury.
• Crystals: Not specific for renal disease, but relevant if obstruction or ethylene glycol toxicity is suspected.
• Cytology: Not routinely indicated unless neoplasia or fungal disease is suspected.

Monitoring Parameters and Their Utility

Serial monitoring in CKD tracks progression and complications. The minimum database at each recheck includes body weight, body condition score, systolic blood pressure, serum creatinine, UPC, and USG. Additional parameters depend on stage and clinical signs.

The MSD Veterinary Manual provides species-specific reference intervals and clinical guidance that should be consulted when interpreting serial values, as normal ranges differ between dogs and cats and by age.

Species and Clinical Context Modifications

The diagnostic approach is not identical across species. Cats with CKD frequently maintain a normal serum creatinine until substantial renal mass is lost, and they are prone to hypokalemia and hyperthyroidism, which can mask or exacerbate azotemia. Dogs more commonly present with glomerular disease and proteinuria. In both species, muscle mass affects creatinine interpretation. A cachectic patient with low muscle mass may have a creatinine in the reference interval despite a markedly reduced GFR. The renal biomarker review highlights that serum creatinine interpretation in domestic species requires adjustment for body condition and muscle mass.

Production animals and exotic species present additional constraints. In cattle and small ruminants, handling stress and recumbency can affect urine collection and blood pressure measurement. Point-of-care analyzers validated for companion animals may not be validated for production species, and reference intervals differ. The WOAH terrestrial animal health standards address disease surveillance and reporting obligations that may apply when renal disease has an infectious etiology, such as leptospirosis.

Equipment availability changes the workup. Practices without in-house blood pressure measurement can still stage CKD by creatinine and UPC, but hypertension will be underdiagnosed. Practices without a centrifuge can perform dipstick and refractometry but cannot reliably identify casts or cellular sediment. The AVMA practice resources provide guidance on laboratory quality assurance and point-of-care testing that supports clinical decision-making when in-house and reference laboratory results are used together.

Documenting Findings

The medical record should include the IRIS stage, proteinuria substage, and blood pressure substage at each visit. Serial creatinine values are plotted or tabulated to identify trends. The UPC and USG are recorded with the collection method and any confounding factors such as hematuria or pyuria. Blood pressure is recorded with the method used, the cuff size, and the patient's position and demeanor. This documentation supports trend analysis, treatment adjustments, and communication with referral centers.

Recognized Complications and Early Detection

Acute kidney injury can propagate damage beyond the nephron. Renohepatic crosstalk describes hepatic dysfunction arising from AKI, with evidence drawn from animal models and clinical data showing effects on synthetic function, the acute phase response, and drug metabolism (Renohepatic crosstalk: does acute kidney injury cause liver dysfunction?). Monitor hepatic enzymes and bilirubin in AKI patients, but recognize that standard liver tests may underestimate the true functional impact. Serial assessment of coagulation times and albumin can detect synthetic failure earlier than transaminase rises alone.

Ischemia-reperfusion injury produces perfusion deficits that persist after the inciting event resolves. Experimental work using arterial spin labeling MRI in mice demonstrates that reduced renal perfusion correlates with histologic tubular injury and functional decline measured by inulin clearance (Acute kidney injury: arterial spin labeling to monitor renal perfusion impairment in mice). In practice, perfusion status is inferred from urine output, blood pressure, and serial creatinine trends. A rising creatinine despite adequate perfusion pressure should prompt investigation for ongoing tubular injury instead of simple prerenal azotaemia.

Nephrotoxic injury follows a predictable temporal pattern. Chemotherapeutic agents such as doxorubicin cause combined hepatorenal toxicity, with histologic hemorrhage and focal necrosis in both organs (Protective effect of berberine on doxorubicin-induced acute hepatorenal toxicity in rats). Similarly, high-dose streptozotocin produces transient elevations in BUN and creatinine alongside marked renal tubular injury on histology (The effect of low versus high dose of streptozotocin in cynomolgus monkeys). When a patient receives a known nephrotoxin, measure creatinine and urine output before administration, at 24 to 48 hours, and again at day 7. Early detection relies on trend analysis, since a single value within the reference interval does not exclude injury.

Common Interpretation Errors

The most frequent error is overinterpreting a single creatinine value without accounting for muscle mass, hydration, and assay variability. A cachectic patient with 50% muscle loss can have a normal creatinine despite substantial functional decline. Correct by combining creatinine with SDMA and urine specific gravity, and by establishing a baseline for serial comparison.

A second error is dismissing an isosthenuric urine specific gravity when BUN and creatinine are normal. Isosthenuria in a hydrated patient indicates that at least two-thirds of nephrons are nonfunctional. This finding alone warrants staging and monitoring even when biochemistry appears unremarkable.

A third error involves proteinuria interpretation. A positive dipstick reading without sediment examination may reflect hematuria or inflammation instead of glomerular disease. Always perform sediment analysis before attributing proteinuria to renal parenchymal damage, and confirm with urine protein:creatinine ratio when the dipstick is positive.

Troubleshooting Table

Evidence Limitations and Referral Criteria

The evidence base for renal biomarkers in veterinary species remains constrained. Conventional tests such as serum creatinine, urea nitrogen, urine protein:creatinine ratio, and urine specific gravity all carry important limitations, and newer markers of glomerular filtration rate and tubular damage are still being validated for earlier detection (Renal biomarkers in domestic species). Expert opinion differs on how aggressively to pursue novel biomarkers in stable patients, and on the optimal frequency of monitoring in early IRIS stage 1 disease. Acknowledge this uncertainty when counseling owners.

Referral is warranted when azotaemia progresses despite appropriate management, when anuria persists beyond 24 hours, when hypertension remains uncontrolled on two agents, or when the diagnostic picture suggests a lesion requiring advanced imaging or biopsy. Laboratory consultation is appropriate when results conflict with clinical findings, when reference interval questions arise, or when method validation concerns affect interpretation. The ASVCP quality assurance guidelines provide a framework for evaluating laboratory performance and reference intervals.

Regulatory reporting obligations vary by jurisdiction. Where zoonotic disease, food animal drug residues, or reportable diseases are suspected, consult the WOAH terrestrial animal health standards and local veterinary authorities. In production animal practice, renal disease may have herd-level implications that require investigation of water quality, feedstuffs, and toxin exposure.

Frequently Asked Questions

How Should I Interpret Renal Tests When I Only Have In-House Chemistry and No Urinalysis Access?

In-house chemistry without urine data limits staging and localization. Serum creatinine and BUN confirm azotaemia but cannot distinguish prerenal, renal, or postrenal causes. Symmetric dimethylarginine (SDMA) may rise earlier than creatinine, but both are filtration markers, not damage localizers. Without urine specific gravity, you cannot confirm inadequate concentrating ability, and without sediment and protein assessment you cannot identify tubular injury or glomerular protein loss. If urinalysis is unavailable, document the limitation, treat the patient's volume status, and refer or send urine to an external laboratory before staging. The ASVCP quality assurance guidelines emphasize that test interpretation depends on method validation and sample quality, so record which analyzer and method produced each result.

When Should I Suspect That Elevated BUN Reflects Non-Renal Disease instead of Kidney Failure?

BUN rises with increased protein intake, gastrointestinal bleeding, catabolism, and hypovolemia, and it falls with hepatic insufficiency or low protein intake. A disproportionate BUN-to-creatinine ratio, normal urine specific gravity, and absence of urinary sediment changes point away from primary renal disease. Prerenal azotaemia should correct within 24 to 48 hours of fluid therapy, failure to correct suggests intrinsic injury. Hepatic causes of low BUN are relevant when synthetic liver function is concurrently impaired, and the bidirectional relationship between kidney injury and hepatic dysfunction is documented in the renohepatic crosstalk literature. Always interpret BUN alongside creatinine, SDMA, urine specific gravity, and physical examination findings before concluding that azotaemia is renal in origin.

What Is the Most Practical Approach When SDMA Is Elevated but Creatinine Remains Within Reference Limits?

An elevated SDMA with normal creatinine suggests reduced glomerular filtration that has not yet produced measurable creatinine accumulation, or a non-renal confounder such as early dehydration or reduced muscle mass. Repeat both tests in two to four weeks, measure urine specific gravity, and assess proteinuria. If SDMA remains elevated with inadequate urine concentration, early chronic kidney disease is likely and IRIS staging should proceed using SDMA-based criteria. Remember that SDMA is not a damage marker, it does not localize injury to glomerulus or tubule. Urinary biomarkers such as low-molecular-weight proteins and enzymes can help localize tubular damage, while high-molecular-weight proteins suggest glomerular injury, as reviewed in renal biomarkers in domestic species. Document the discordance clearly in the record.

How Do I Adjust My Diagnostic Plan for a Cat With Suspected Chronic Kidney Disease and Concurrent Hyperthyroidism?

Hyperthyroidism increases glomerular filtration rate, which can mask azotaemia by lowering creatinine and SDMA. A cat with normal renal tests but inadequate urine concentration may still have significant structural kidney disease. Conversely, treatment of hyperthyroidism can unmask azotaemia as filtration falls toward true baseline. Measure total thyroxine, urine specific gravity, and blood pressure in every older cat with suspected renal disease. Recheck renal biochemistry four to eight weeks after starting antithyroid therapy. The MSD Veterinary Manual provides species-specific guidance on interpreting renal tests in the context of concurrent endocrinopathy. Do not stage chronic kidney disease from a single pre-treatment sample, and document that staging reflects the post-treatment state.

What Should I Record in the Medical Record When Renal Test Results Are Ambiguous or Conflicting?

Record the analyzer and method, sample quality, and any hemolysis or lipaemia that could affect results. State the clinical question, the tests performed, and the interpretation with the reasoning. If SDMA and creatinine disagree, note the possible explanations and the planned recheck interval. Record urine collection method, specific gravity, dipstick findings, sediment description, and whether proteinuria was quantified by urine protein-to-creatinine ratio. If you referred samples to an external laboratory, note the accession number. The AVMA practice resources emphasize that medical records must support continuity of care and defend clinical decisions. When findings are ambiguous, document the differential diagnoses and the monitoring plan instead of forcing a single conclusion.

How Should I Explain Discordant Renal Test Results to a Client Without Undermining Their Confidence in the Diagnosis?

Use plain language that separates filtration from damage. Explain that the kidneys filter waste and also hold onto protein, and that different tests measure different jobs. If SDMA is high but creatinine is normal, say the kidneys are filtering less efficiently than expected and that repeat testing will show whether this is stable or progressive. Avoid giving a definitive prognosis from one sample. Explain that urine testing tells us whether the kidneys are concentrating urine and leaking protein, which changes the treatment plan. The WOAH terrestrial animal health standards illustrate how standardized diagnostic criteria support consistent decision-making across settings, and the same principle applies in practice: use the same tests and criteria at each recheck so trends are meaningful. Offer a written summary of the numbers and the next recheck date.

Related Clinical & Scientific Guides

• Peripheral Blood Smear Evaluation: A Step-by-Step Guide
• Reticulocyte Counts in Veterinary Medicine: Clinical Utility and Interpretation
• Cerebrospinal Fluid Analysis in Veterinary Neurology: Collection and Interpretation

References and Further Reading

• Renal biomarkers in domestic species.. 2016.
• Renohepatic crosstalk: does acute kidney injury cause liver dysfunction?. 2013.
• Acute kidney injury: arterial spin labeling to monitor renal perfusion impairment in mice-comparison with histopathologic results and renal function.. 2014.
• Protective effect of berberine on doxorubicin‑induced acute hepatorenal toxicity in rats.. 2016.
• The effect of low versus high dose of streptozotocin in cynomolgus monkeys (Macaca fascilularis).. 2003.
• Metabolic Modulation of Clear-cell Renal Cell Carcinoma with Dichloroacetate, an Inhibitor of Pyruvate Dehydrogenase Kinase.. 2016.
• American Society for Veterinary Clinical Pathology Guidelines. American Society for Veterinary Clinical Pathology.
• MSD Veterinary Manual, Professional Edition. MSD Veterinary Manual.
• American Veterinary Medical Association Practice Resources. American Veterinary Medical Association.

Related Articles

• Monitoring Renal Function in Chronic Kidney Disease: Serial Biochemistry
• Urinalysis in Veterinary Practice: From Collection to Interpretation
• Interpreting the Canine CBC: A Diagnostic Approach
• Monitoring Cardiac Biomarkers in Heart Failure Management
• Platelet Function Testing in Veterinary Patients: Clinical Applications

This article is educational professional reference material for veterinary audiences. It is not a substitute for veterinary diagnosis, individual clinical judgment, current product labeling, or applicable regulatory requirements.